Chapter 4e Internal Medicine
Transcript of Chapter 4e Internal Medicine
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4.5 Internal Medicine
Sushama Rich, MD
Cardiovascular System
Approach to the Cardiac Patient
Most common presenting symptoms:
Chest Pain
Chest pain of cardiac origin is commonly these types:
Pericardial
Anginal
Myocardial infarction
Aortic dissection
Pericardial pain
Sharp pain that radiates to the trapezius and is aggravated by breathing. Relieved by leaning forward and
remaining still.
Causes Pericarditis
Diagnosis
On auscultation shows pericardial friction rub
ECG shows ST segment elevation
Anginal pain
Substernal chest pain that is squeezing in nature radiates to the jaw, left arm, or left shoulder.
It is aggravated or brought on by exercise.
Relieved by rest or nitroglycerin
Chest pain usually never lasts more than 20 minutes
Diagnosis
Usually clinical ECG shows ST segment changes
Myocardial Infarction
Same as anginal pain
Duration usually greater than 20 minutes
Not relieved by rest
Diagnosis
ECG: ST segment changes
Blood tests show CPK-MB, Troponin
Aortic dissection
Sudden onset, tearing type of pain that radiates to the back mid scapular
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Cardiac Dyspnea
Cardiac dyspnea is labored breathing that is caused by edema in the bronchial walls and stiffening of the lungs
due to alveolar edema.
Dyspnea is due to a reduction in cardiac output
Dyspnea is aggravated by exercise and relieved sometimes by rest
Causes of cardiac dyspnea
Congestive heart failure
Coronary artery disease
Types of cardiac dyspnea
Orthopnea: dyspnea that occurs in the recumbent position due to increased paroxysmal nocturnal dyspnea
Paroxysmal nocturnal dyspnea: dyspnea that wakes a patient up in the middle of the night
Palpitations
Palpitations are the perception of ones own heart beat. Most common cardiac cause is arrhythmias.
Diagnostic and cardiovascular procedures
Chest X-ray
Shows
Heart size
Heart shape
Great vessels
Electrocardiogram
Can diagnose old or current heart attacks
Disturbances of heart rhythm
Detects thickening of the wall
Holter Monitoring
Uses a portable recording device worn by the patient under the clothing for 24 hours. This procedure is used for:
Documents arrhythmias
Classifies arrhythmias Diagnoses silent ischemia
Assess results of antiarrhythmic drugs
Exercise Stress Test
Used to:
Diagnose CAD
Evaluate known CAD
Contra-indications
A M.I.-within the last 48 hours
Severe aortic stenosis
Congestive heart failure
Echocardiography
Echocardiography reveals the anatomy of the heart. This technique is use for:
Valvular disease
Congenital heart disease
Function of the heart muscle
Flow of blood- this can be seen by color Doppler (blue and red)
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Coronary Angiography
Coronary angiography is the best test for CAD
Vessels as small as 1mm can be visualized
Any occlusion of the artery is seen as narrowing, beading or occlusion of the vessel
Myocardial perfusion
Myocardial perfusion imaging uses radioactive thallium. Indications
Initial evaluation of patients
Prognosis after an acute M.I.
To detect extent of scarring after an acute M.I.
MUGA Scan Equilibrium Radionuclide Angiography
After receiving a small injection of a radioisotope, the patient lies on a table and multiple images are recorded
by scintillation camera.
Uses
Evaluates cardiac function
Measures ejection fraction
Show the contraction of different regions of the heart
Coronary Artery Diseases
Two types of coronary artery disease:
Atherosclerotic coronary artery disease (ASCAD)
Non atherosclerotocic coronary artery disease (NASCAD)
Atherosclerotic Coronary Artery Disease (ASCAD)
Definition
The basic lesion is atherosclerosis of the coronary arteries. The pathological hallmark of this disease is athero-
sclerotic plaque. Plaque is made up of hypertrophied intimal smooth muscle cells, lipids, and a fibrous cap.
Risk factors for the development of ASCAD
Increases with age
Gender: more common in men
Serum cholesterol: high levels of LDL. This is the single most important risk factor, low levels of HDL
Smoking
Hypertension
Diabetes mellitus
Family history
Oral contraceptives
Pathogenesis of ASCAD
As the typical plaque develops, it begins to occlude the coronary arteries; this leads to a reduction of blood flow
to the myocardium. In order for ischemic symptoms to develop at least 70% of the coronary artery has to be occlud-
ed by the plaque. A variety of factors influence the clinical course of CAD, like the length of the lesion, vasomotor
tone, rupture of the plaque, erosion of the plaque and ultimately thrombus formation.
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Clinical Features of ASCAD
The most common feature of ischemia to the myocardium is angina pectoris
Ischemia could proceed without any symptoms to an M.I.
Ischemia may cause sudden death
Angina could present in three forms.
Stable angina Chest pain or pressure produced by exertion
Radiates to the jaw or arm
Brought on by exercise
Relieved by rest
Associated with exertional dyspnea
Does not last more than 20 minutes
If pain lasts more than 20-30 minutes and is not relieved by nitro, suspect M.I.
Unstable angina
Chest pain same as above
It is progressive in nature: The episodes are more frequent and last longer but never more than 20 minutes
It is of increasing severity, duration, or frequency Printzmetals angina
The hallmark of this disease is S-T segment elevation on ECG
S-T segment elevation indicates transmural infarction of the myocardium
It is classically caused by coronary vasospasm that occurs near an atherosclerotic plaque
It more commonly affects women; it occurs more often at night, not associated with exertion
There is no increase serum markers for an M.I.
Diagnosis of Angina
Clinical symptoms are key
Resting ECG: is usually normal between episodes
Sometimes one may see new horizontal or down sloping S-T segment
New T wave inversion
S-T segment elevations indicates variant angina
Exercise stress test: The appearance of horizontal or down sloping of S-T segment depression of more than 1
mm indicates ischemia
Exercise stress test associated with thallium stress test is much more valuable
Coronary angiography is done for confirming a suspicion, diagnosis, risk stratification, assessment of CABG
or angioplasty
Treatment of Angina
Nitrates
B-adrenergic blockers: limit myocardial oxygen demand
Calcium antagonists: prevent coronary spasm, hence ideal for variant angina
PCTA: percutaneous transluminal angioplasty
Rotational atherectomy
Coronary artery bypass surgery: indicated for multi-vessel disease
Beta blockers should not be used in variant angina because blockade of the alpha receptors cause alpha
receptor mediated vasoconstriction
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Myocardial infarction
Occurs when there is 100% occlusion of the coronary artery.
Pathogenesis
Acute M.I is almost always associated with a thrombus superimposed upon a significant plaque
It takes at least 20 minutes of ischemia to cause an irreversible injury
Most often occurs in the morning when there is decreased adrenergic activity Myocardial necrosis begins in the sub-endocardium and spreads to the epicardium
Most common artery to be blocked is the left anterior descending
Table 1. Classification of Myocardial Infarction
Characteristic Q-Wave MI Non-Q Wave MI
Prevalence 47% 53%
Complete coronary obstruction 80-90% 15-25%
Elevated ST-T segment 80% 25%
Depressed ST-T segment 20% 75%
Postinfarction angina 15-25% 30-40%
Early reinfarction 5-8% 15-25%Infarct size Moderate to large Usually small
Acute complications Common Uncommon
Therapy
Thrombolysis Indicated Not indicated
Beta Blockers Indicated Not indicated
Clinical Features
Chest pain for more than 30 minutes
Associated symptoms: dyspnea, diaphoresis, nausea, vomiting, palpitations, and light-headedness.
Symptoms simulate: GI-upset
Physical Exam Signs of ischemia: S4, new MR murmur
Signs of heart failure: increased JVP, crackles in lung fields, S3
Diagnostic Studies
ECG: diagnostic in 85% of cases
ST segment elevation, Q waves, T wave inversion
Serum markers: CPK MB is increased within six to ten hours post MI, troponin I increases within 6-10 hours
post MI, LDH1 increases within 48-72 hours
Echocardiogram: New wall motion abnormality
Treatment
Treatment of pain: Nitroglycerine, morphine sulfate
Thrombolysis
Indications for thrombolytic therapy are the following:
Chest pain
ECG: ST segment elevation
Less than 12 hours from onset
No contra indication
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Absolute contra-indications for thrombolytic therapy:
Active internal bleeding
Suspected aortic dissection
Recent head trauma
Blood pressure greater than 200/120
Pregnancy
CVA
Trauma or surgery within two weeks
Relative contra-indications:
Active peptic ulcer disease
Known bleeding diathesis
Menstruation
Prolonged CPR
Drugs used for thrombolytic therapy:
Alteplase (TPA): Fifteen mg IV-bolus, .75 mg per kilogram over 30 minutes, 5 mg per kilogram over 60
minutes
Streptokinase (SK): 1.5 Mu IV over 30-60 minutes
Reteplase (RPA): 10 u IV repeat in 30 minutes
Drugs used for arrhythmias
Prophylactic Lidocaine
Procainamide for acute recalcitrant arrhythmias
Treatment of conduction disturbances
Atropine
Treatment of heart failure
Diuretics for mild congestive heart failure
Digitaliscontroversial
Treatment of mitral regurgitation and acute ventricular septal defect
Arteriolar vasodilator therapy Intra-aortic balloon pumping
Adjunct therapy
Beta-blockers reduce early mortality by reducing ventricular arrhythmias
ACE inhibitors reduce the extent of remodeling and incidents of late mortality
Anti-coagulants: heparin
Aspirin
Diltiazem: for non Q wave infarcts
Angioplasty
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Complications of MI
Ventricular arrhythmias
Acute conduction abnormalities
Ventricular aneurysm
Pump failure
Mitral regurgitation Ventricular septal defect
Cardiac rupture
Left ventricular aneurysm
Dresslers syndrome occurs in 2-10 weeks post MI. Presents as fever, malaise, pericarditis and pleuritis
Pericarditis
Prognosis
Depends on the number of vessels affected. Extent of left ventricular damage
Non-atherosclerotic Coronary Artery Disease
Causes Coronary embolism occurs in infective endocarditis, atrial fibrillation
Collagen vascular disease affects medium-sized arteries. Ex: SLE RA, Wegeners granulomatosis
Radiation therapy
Cardiac transplantation
Heart Failure
Heart failure is the inability of the heart to pump blood to meet the oxygen requirement of the body tissues.
Heart failure is a syndrome of many diseases that interfere with cardiac function. There are two types of heart fail-
ure, low output and high output. Low-output failure occurs due to reduction in the cardiac output. High-output
failure occurs due to an increase in cardiac output.
Etiology Ischemic heart disease
Hypertensive heart disease
Cardiomyopathies
Valvular heart disease
Pericardial disease
High output failure: AI, MR, VSD, AV fistulas, severe anemia, sepsis, thyrotoxicosis, beri beri
Pathophysiology
Systolic dysfunction: Could be of two types, decrease in contractility or increased after load
Decreased contractility occurs due to MI valvular heart disease, hypertension, cardiomyopathies
Increased after load occurs due to hypertension, aortic stenosis or dilated cardiomyopathy and valvular
regurgitation Diastolic dysfunction: Hypertrophic cardiomyopathy may occur in hypertension and amyloidosis
Descriptive Terminology
High-output failure occurs due to increased cardiac output. Example, chronic severe anemia causes volume
overload
Left-sided failure occurs when the left ventricle is failing. Example, MI
Right-sided failure: Most common cause is left ventricular failure. It may also occur due to COPDs in which
case it is called corpulmonale
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Clinical Features
Dyspnea
Orthopnea that leads to nocturnal cough
Paroxysmal nocturnal dyspnea
Nocturia
Edema
Anorexia
Right upper quadrant pain
Fatigue
Physical Signs
Acute heart failure
Hypo or hypertension, tachycardia, diaphoresis, cyanosis, cold and pale extremities
Left-sided failure
Pulmonary rales, cardiac murmurs, tachypnea
Right-sided failure
Increased JVP, pleural effusions, congestive hepatomegaly, ascites, jaundice, peripheral edema
Diagnosis
Chest X-ray shows pulmonary edema, bilateral pleural effusions
Echocardiogram: Decreased ejection fraction and increased chamber size indicate systolic dysfunction, hyper-
trophy and or abnormal inflow across the mitral valve indicates diastolic dysfunction
Pulmonary artery catheterization: Increased PCWP, decreased CO and increased SVR indicates low-output
failure
Classification
Class 1: Symptomatic only with greater than ordinary activity
Class 2: Symptomatic with ordinary activity
Class 3: Symptomatic with minimal activity Class 4: Symptomatic at rest
Treatment
Diet: reduction in sodium
Diuretics: Loop or thiazide diuretics
ACE inhibitors
Digoxin
Beta-blockers
Spironolactone
Anti-coagulants
Cardiomyopathies
Cardiomyopathies is myocardial dysfunction that is not due to ischemic valvular hypertensive or congenital
heart disease. Types of cardiomyopathy:
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
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Dilated cardiomyopathy: Occurs due to ventricular dilation with decrease in contractile function of the left,
right or both ventricles in the absence of pressure overload, volume overload or CAD. It almost always results in
congestive heart failure.
Etiologies
Ischemia
Valvular disease: Chronic AI or MR, hypertension
Toxic: most common cause is alcohol induced
Drug therapy: Example, Doxirubicin therapy
Infectious: Example, viral HIV
Idiopathic
Endocrine disorders: Example, thyrotoxicosis, hypothyroidism, acromegaly
Metabolic disorders: Example, hypophosphotemia, hypocalcemia, thyamine deficiency
Hemoglobinopathies: Example, sickle cell anemia, thalassemia
Collagen vascular disease: Example, SLE, and scleroderma
Clinical Features
Include both left and right-sided heart failure Chest pain
Physical Signs
Signs of left-sided heart failure
Diagnosis
History
Stress test
Cardiac catheterization
Lab studies
Echocardiography is the most important test that reveals dilated, poorly contracting left and right ventricles
Treatment
Standard heart failure therapy
Immuno suppressants
Cardiac transplantation
Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy is a disorder in which there is hypertrophied septum, mitral valve prolapse, and
left ventricular outflow obstruction.
Etiology
Inherited autosomal dominant Some sporadic cases are known to occur
Specific abnormalities of cardiac myosin occurs
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Pathophysiology
Hypertrophied septum encroaches upon the left ventricular outflow
Obstruction of the anterior leaflet of the mitral valve
Systolic anterior motion of the anterior leaflet of the mitral valve
Which then leads to papillary muscle displacement
Diastolic dysfunction, the left ventricle is so stiff that it does not fill properly during diastole Decreased coronary perfusion occurs
Leads to syncope
Clinical Features
Dyspnea
Angina
Syncope
Arrhythmias
Palpitations
Congestive heart failure
Physical Examination
Murmur: mid- to late-holosystolic murmur
The murmur is reduced in intensity with the valsalva murmur, and increased in intensity from squatting
Carotid upstroke has a spike and a dome character to it
Diagnosis
ECG; left ventricular hypertrophy
CXR; cardiomegaly
Echocardiogram is the gold standard for diagnosis: shows septal hypertrophy, mitral regurgitation, outflow
tract obstruction
Treatment
Medical Therapy
Beta blockers
Calcium channel blockers
Digitalis: only in the end stage of the disease
Surgical treatment
Myomectomy; surgical reduction of the septum
Mitral valve replacement
Pacemaker implantation
Restrictive Cardiomyopathy
Definition: Impaired ventricular filling due to decreased compliance caused by increased stiffness of the wall
Etiology
Infiltrative diseases; examples are amyloidosis, hemochromatosis, carcinoid syndrome, sarcoidosis, idiopathic
eosinophilia
Metastatic diseases
Radiation therapy
Idiopathic
Scleroderma
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Pathology
Increased diastolic stiffness
Systolic function is usually normal in the early stages
Left ventricular pressure is above normal
Systolic function is compromised in the late stages
Decreased ventricular cavity size Decreased cardiac output
Clinical Features
Right-sided failure is greater than left-sided failure
Peripheral edema
Dyspnea
Refractory to treatment with diuretics
Thromboembolic events
Physical Examination
Increased JVP
Cardiac S3 and S4 Congestive hepatomegaly
Ascites
Jaundice
Peripheral Edema
Diagnostic Studies
Chest X-ray shows normal chamber size, enlarged atria, pulmonary congestion
ECG
Echo shows symmetrical wall thickening, increased diastolic end pressure, decreased atrial filling
Treatment
Treat underlying disease
Symptomatic therapy with diuretics
Valvular Disease
Aortic Stenosis
Etiology
Congenital (e.g. bicuspid valve): In young and middle-aged adults, bicuspid aortic valve with progressive
scarring and calcification is the most common cause
Rheumatic Disease Degeneration and calcification of a tricuspid valve
Aortic stenosis is more common in men
Disease Process
The outflow obstruction leads to left ventricular hypertrophy
Symptoms
Symptoms are not usually present until the obstruction is advanced
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Cardiac symptoms
Angina Pectoris
Syncope
Dyspnea
Physical Findings
Ejection murmur is typically harsh and is often loud. The duration of the murmur is proportional to the
severity of the obstruction
The carotid pulse is characteristically reduced in amplitude and prolonged in duration
Diagnosis
Echocardiography and the Doppler confirms the diagnosis
The Doppler flow velocity can determine the severity
Treatment
Surgery for patients with cardiac symptoms and severe aortic stenosis
Avoid vigorous activities
Cardiac catheterization for patients with severe aortic stenosis
Chronic Aortic Regurgitation
Etiology
Bicuspid Aortic valve
Aortic root dilatation
Endocarditis
Associated with some connective tissue disorders. (e.g. Marfans Syndrome)
Disease Process
Aortic regurgitation results in a volume overload of the LV with ventricular dilatation. The stroke volume is
increased as the LV ejects both the forward output and the blood that regurgitated into the ventricle duringdiastole
Symptoms
Palpitations/pounding in the chest or head
Dyspnea due to elevated pulmonary venous pressure
Angina pectoris due to decreased diastolic coronary perfusion
Physical Findings
Wide pulse pressure
Systolic ejection murmur
Third heart sound
Diagnosis
Endocardiography can determine the cause of aortic regurgitation in many patients
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Treatment
Surgery for patients with LV systolic dysfunction and onset of symptoms
Oral vasodilator therapy for asymptomatic patients with significant aortic regurgitation and normal systolic
function. By decreasing systemic resistance regugitant volume is reduced
Acute Aortic RegurgitationEtiology
Infective endocarditis
Prosthetic aortic valve dysfunction
Proximal dissection of the aorta
Disease Process
Severe acute condition places a volume overload on a left ventricle that has not had the time to dilate in a
compensatory manner. The increased ventricular diastolic pressure leads to left atrial pressure and pul-
monary congestion
Physical Findings
Sinus tachycardia is often present
Diastolic murmur may be less prominent and shorter in duration
Third heart sound gallop can be heard
Diagnosis
Endocardiography and Doppler assess the status of Aortic regurgitation, its cause, and the underlying ven-
tricular function
Treatment
Vasodilator therapy
IV nitroprusside for severe heart failure
Surgical therapy is the definitive treatment
Mitral Stenosis
Etiology
Rheumatic Fever
Occurs twice as frequently in female patients as male
Disease Process
Progressive thickening of the valve leaflets and fusion of the commisures. Calcification contributes to the
valve immobility and stenosis
The chora tendinae also may thicken and fuse
The valve scarring progresses slowly before symptoms arise. Elevated left atrial pressure leads to pulmonaryartery hypertension that can provoke RV failure and functional tricuspid regurgitation
Symptoms
Exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea due to pulmonary venous congestion
Fatigue and weakness when the cardiac output decreases
Symptom onset is most common in the third or the fourth decade of life
These patients, who may get atrial fibrillation, a common complication, may not tolerate increased heart rate
Embolism from enlarged left atrium can cause stroke, especially when atrial fibrillation is present
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Physical Findings
Left atrium is enlarged because mitral stenosis increases the left atrial pressure
Loud first heart sound
As the severity of mitral stenosis increases, the interval between the 2nd heart sound and opening snap
decreases
Diagnosis Echocardiography can detect mitral valve thickening, provide information about valve mobility and the
degree of calcification.
Treatment
-blockers
Control atrial fibrillation
Anticoagulants to decrease the risk of thromboembolism
Percutaneous mitral valve balloon valvuloplasty
Valve replacement
Mitral Regurgitation
Etiology
Mitral valve prolapse
Ischemic heart disease can cause papillary muscle ischemia
Left ventricular (LV) dilation
Mitral Annulus calcification
Rheumatic heart disease
Acute mitral regurgitation can result from the rupture of chorda tendinae or papillary muscle
Disease Process
Chronic mitral regurgitation produces a volume overload
Left atrium is moderately enlarged and there is elevation of left atrial pressure, which can lead to pulmonary
congestion and dyspnea
Physical Findings
Holocystic murmur is characteristic, which begins immediately after a soft 1st heart sound. It is high-pitched
Diagnosis
Echocardiography can assess mitral valve structure, cardiac chamber size, and left ventricle function
Doppler assesses the severity of the mitral regurgitation
Treatment
Vasodilater therapy to decrease the afterload (e.g. ACE inhibitors)
Valve replacement
Mitral Valve Prolapse (MVP)Etiology
MVP is common and can cause mitral regurgitation ranging from trivial to severe
Can be isolated, or associated with connective tissue diseases (e.g. Marfans)
More common in women
MVP can be inherited (autosomal dominant)
MVP is benign in most patients
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Disease Process
Mitral valve in these patients is usually large, floppy, and redundant with elongated chorda tendinae
Middle-aged or older men may be more likely to develop severe regurgitation or complications
Complications
Ineffective endocarditis
Cardiac arrhythmia
Thromboembolism
Symptoms
Most MVP patients are asymptomatic, but the following symptoms can be present:
Atypical chest pain
Palpitations
Fatigue
Anxiety
Postural phenomena
Neuropsychiatric symptoms
Diagnosis
Echocardiography is used to confirm the diagnosis
Treatment
Antibiotic endocarditis prophylaxis in all MVP patients with structural valve changes and/or murmur of
regurgitation
-blockers
Pericardial Diseases
Pericarditis and pericardial effusion
Pericardial tamponade Constrictive pericarditis
Pericarditis is an inflammation of the pericardium. Pericardial effusion is an accumulation of fluid within the
pericardial cavity.
Etiologies
Infectious
Viral: Coxsackie B virus, echovirus, adenovirus, EBV, VZV, HIV
Bacterial: (From endocarditis, pneumonia or cardiac surgery), S. Pneumoniae, S. Aureus, and TB
Non-infectious
Idiopathic
Uremia Acute MI
Post MI: Dresslers syndrome
Post pericardiotomy
Neoplastic: Lung, breast, renal cell
Trauma: Chest trauma
Pericardial effusion without pericarditis, CHF, cirrhosis
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Clinical Features
Chest pain: Burning, stabbing increased by breathing, reduced by leaning forward, radiates to the trapezius
Fever
Physical Exam
Pericardial friction rub is the gold standard for clinical diagnosis
Pericardial effusion will cause distant heart sounds, dullness over the left posterior lung field (Ewarts sign due
to compressive atelectasis)
Diagnostic Studies
ST segment elevation throughout the ECG, depression of the PR segment is diagnostic and unique to peri-
carditis
Echocardiography will show pericardial effusion. Echo-free space between the two layers of the pericardium
Chest X-ray: Water bottle appearance of the heart
Treatment
NSAIDS
Steroids for refractory idiopathic disease Treat underlying cause
Cardiac Tamponade
Cardiac tamponade is a life-threatening condition due to a rapid development of pericardial effusion that is
compressing the heart.
Pathophysiology
The heart cannot fill adequately
Increased intra-pericardial pressure
Diastolic pressure is elevated
Pulsus paradoxus: Inspiration causes a decrease in intra-pericardial and right atrial pressures which leads toan increase in venous return, which leads to increased RV size which leads to septal shift to the left which
leads to decrease in left ventricular stroke volume and output
Clinical Features
Dyspnea on exertion
Fatigue
Orthopnea
Physical Exam
Pulsus paradoxus: When the systolic blood pressure falls more than 10 mm of mercury during inspiration.
This implies that stroke volume is falling during inspiration due to compression
Neck vein distension
Diagnosis
Echocardiogram shows effusion
Treatment
Emergency pericardiocentesis
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Constrictive Pericarditis
Constrictive pericarditis is caused by diffuse thickening of the pericardium due to inflammatory process
Etiology
Post viral
Radiation
Uremia
TB
Idiopathic
Post surgical
Clinical Features
Dyspnea
Orthopnea
Ascites
Edema
Jaundice
Typical symptoms are right-sided heart failure
Diagnosis
ECG shows atrial arrhythmias
Echocardiography is not as valuable
MRI is capable of measuring pericardial thickness
Treatment
Surgical removal of the pericardium
Aortic Diseases
Aneurysms of the aorta Aortic dissection
Aneurysms of the Aorta
An aneurysm of the aorta is permanent dilation of an artery due to weakness of the wall.
Etiology of Aortic Aneurysms
Aneurysms of the ascending aorta is caused by syphilis, Marfans syndrome, and cystic medial necrosis
Aneurysms of the abdominal aorta are caused by atherosclerosis. This type increases with age, smoking, and
hypertension and has increased incidence in men. The most common site is at the bifurcation of the aorta
Aneurysms of the femoral artery occur due to mycotic infections. It most often occurs in IV drug users
Pathophysiology
Atherosclerosis is the hallmark of aneurysms
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Clinical Features
Small aneurysms are asymptomatic. Large aneurysms cause back pain and pulsating sensations
Blue toe syndrome: sudden occurrence of a very painful blue toe most commonly caused by emboli
Aortic aneurysms can rupture causing massive bleeding, syncope, hypotension and diarrhea with Tenessmus
Musculoskeletal pain
Diagnosis
Most of them are found incidentally on physical exam
Ultrasound is the gold standard
CT scan is used to localize ruptures
Aortograms are rarely used
Treatment
Aneurysms less than 4 cm are usually watched
Aneurysms greater than 5 cm or threat of ruptureconsider surgery
Aortic Dissection
Aortic dissection occurs when the tunica intima tears and blood dissects along the media.
Etiology
Aneurysm of the ascending aorta is most commonly caused by hypertensive aneurysm
Dissection of the descending aorta occurs due to rupture of an atherosclerotic plaque
Blunt trauma can cause either an ascending or a descending aneurysm
Clinical Features
Crushing chest pain that radiates to the back and felt between the scapula
Symptoms of aortic insufficiency may occur
Diagnosis
Murmur of aortic insufficiency
Chest X-ray will show widened media stinum
CT scan confirms diagnosis
Treatment
Stabilize hypotension
Lower systolic blood pressuresurgery
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Co
mmonLaboratoryValues
Age
WBCCo
unt
RBCCount
Hemoglobin
Hematocrit
MCH
MCHC
MCV
RDW
(cells/mm
3)
(106/L)
(g/dl)
(%)
(pg)
(g/dl)
(m
3)
[Sl:109/L]
[Sl:1012/L]
[Sl:g/L]
[Sl:pg]
[Sl:g/L]3
[Sl:fL]
Adultmale
4,500-1
1,000
4.73-5.4
9
14.4
0-16.60
42.9-49.1
27-31
33-37
76-100
11.5-14.5
AdultFemale
4,000-1
1,000
4.1-4.87
12.2-14.7
37.9-43.9
27-31
33-37
76-100
11.5-14.5
Age
PlateletCount
Lymphocytes
Neutrophils,
Neutrophils,
Eosin
ophils
Basophils
Monocytes
(103/L)
Total
Band
Segmented
(%W
BC)
(%WBC)
(%
WBC)
(%WBC)
(%
WBC)
(%WBC)
AdultMale
238,000
34%
3.0%
56%
2
.7%
0.5%
4%
AdultFemale
270,000
34%
3.0%
56%
2
.7%
0/5%
4%
Increasedin
Decreasedin
Leukemiasafter
splenectomy,acute
hemorrh
age,
leukemia,
polycyth
emiavera
Anyviral
infection,
AIDS,MMR,
Acuteand
chronic
lymphocytic
leukemias
Severeexercise,
labor,
newborns,
bacterial
infections,
leukemias,non-
infectivetissue
damage
NAACP
Neo
plasms,
allergies,
Add
isons
dise
ase,collagen
vasculardisease,
parasites
Chronic
myeloid
leukemia
Bac
terial
infection,
sub
acute
bac
terial
end
ocarditis
,ch
ronic
infections,
leukemia
Disseminated
intra-vascular
coagulation,
TTP,ITP
,
eclampsiaand
pre-eclampsia
Pancytopenia,
aplastic
anemia,
neutropenia,
severe
infections,
severe
osteomyelitis
Stress,burns,
trauma,
chemotherapy
Steroids,stress,
Cushings
syndrome
Acute
rheumatic
fever,lobar
pneumonia,
steroidtherapy,
stress,
thyrotoxicosis